Abstract

Chronic hypertension (CH) is a common disorder occurring in approximately 1-5% of pregnant women. Many studies emphasize that the development of superimposed preeclampsia (PE) is associated with high rates of adverse pregnancy outcome. Accurate prediction of women at risk for PE is crucial to judicious allocation of monitoring resources and use of preventive treatment, in order to improve maternal and neonatal outcome. Recent systematic review and meta-analysis showed that mean arterial pressure (MAP) is a better predictor for pre-eclampsia than systolic blood pressure and diastolic blood pressure To detect the value of MAP in the first and second trimesters to predict PE in women with CH. To determine if MAP, assessed in the second trimester, can increase the predictive value for PE of II trimester UtA PI. Cohort study on 100 consecutive singleton pregnancies complicated with CH referred to our Department from January 2008 to June 2011. Blood pressure was measured by a mercury sphygmomanometer at 11-14+6w and 23+0-25+6w, MAP was calculated. Doppler-velocimetry was performed at 23+0-25+6w, mean UtA PI was calculated. PE and CH were defined according to ISSHP criteria. Clinical and perinatal outcomes were reviewed. Receiver-operating characteristic (ROC) curves were used to determine the predictive ability of I and II trimesters MAP and II trimester mean UtA PI for subsequent development of PE. Logistic regression analysis was run to assess the additional value of II trimester MAP to II trimester UtA PI. Mean maternal age was 36 years (SD ±5yy); mean Body mass Index was 24Kg/mq (SD ±5Kg/mq); GA at I Trimester evaluation was 11+4w (SD ±1+5w); I trimester MAP was 100.46mmHg (mean, SD ±9.94mmHg); GA at Doppler and II trimester MAP was 24+4w (SD ±4dd); II trimester MAP 97.53mmHg (mean, SD ±10.27mmHg). Nineteen cases of PE were observed. Seventy patients were under prophylactic ASA 100mg oid. Fifty-two patients were under anti-hypertensive therapy from the first trimester. No differences in prevalence of PE were observed between patients in and out prophylactic treatment, as well as no differences in prevalence of PE were observed between patients under anti-hypertensive treatment or not. The prediction of subsequent development of PE, expressed as the area under ROC curve, was 0.469 (95% CI 0.34-0.59) for I trimester MAP; 0.659 (95% CI 0.55-0.76) for II trimester MAP; 0.748 (95% CI 0.65-0.83) for II trimester mean UtA PI; GA at delivery was 37+4w(mean, SD ±3+2w); mean BW was 2958g (SD ±735g); BW percentile was 38 (mean SD ±29 percentiles); mean BW z-Score was -0.63 (SD ±1.6). Logistic regression analysis showed that MAP does not increase the predictive ability of II trimester UtA PI in women with CH. In our findings, MAP seems not to be a good predictor for subsequent development of PE in women with CH, moreover, it seems to be not useful to increase the predictive value for PE of II trimester UtA PI. II trimester UtA PI has been confirmed to be the best predictor for subsequent development of PE.

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